Plant Responses to Cadmium

Information on molecular mechanisms and signaling events underlying plant transcriptional responses to Cd is rather limited as compared to research in the field of cadmium toxicity. The mechanism by which Cd modulates the levels of expression of most genes is not clearly understood, while our knowledge of global changes in the expression of Cd-responsive genes is also limited. A number of studies have been carried out involving both small-scale experiments and whole-genome approaches. Their findings suggest that gene expression is time- rather than dose-regulated in response to Cd and is differentially regulated in roots and leaves (Herbette et al. 2006; Ogawa et al. 2009). Genes regulated by cadmium can be categorized into different protein groups in terms of photosynthetic processes, signal transduction, and transcriptional regulation, cellular defenses, ROS detoxification and repair, hydric balance, metal transport, cell wall metabolism, sulfate and GSH metabolism and protein degradation.

5.1 Photosynthesis Regulation

The decrease in chlorophyll content has been considered to be one of the early symptoms of cadmium toxicity. The inhibition of chlorophyll biosynthesis has been suggested to be a primary event in Cd toxicity (Baryla et al. 2001). A substantial number of genes involved in photosynthesis were downregulated in the leaves of Arabidopsis plants grown with 5-50 mM Cd. For example, the genes involved in the photochemical process of photosynthesis, such as the chlorophyll synthesis pathway, glutamyl tRNA reductase, hydroxymethylbilane synthase, and Mg chelatase, some proteins of PSI and PS II, electron transporters, enzymes involved in Calvin cycle and Rubisco are downregulated (Herbette et al. 2006). Genes encoding enzymes in the pentose phosphate pathway were also downregulated by Cd (Herbette et al. 2006) . These results have been corroborated by proteomic approaches (Älvarez et al. 2009) and correlate with the reduction observed in the photosynthesis net rates for different plant species (Sandalio et al. 2001; Faller et al. 2005). Downregulation of photosynthesis-related genes is a primary response under different stress conditions probably to avoid oxi-dative damage (Mittler 2002) .

5.2 Signal Transduction and Transcriptional Regulation

Numerous genes involved in signal transduction were regulated in response to Cd in different plant species showing that signal transduction pathways are rapidly activated by the presence of Cd (Suzuki et al. 2001; Herbette et al. 2006; Ogawa et al. 2009). These include genes encoding mitogen-activated protein kinases (MAPKs), calmodulins and calcium-dependent protein kinases (CDPKs) (Suzuki et al. 2001; Herbette et al. 2006; Ogawa et al. 2009), which suggests that Cd interferes with the Ca2+ signaling pathway, as demonstrated by Rodríguez-Serrano et al. (2009). MAPKs and CDPKs are involved in biotic and abiotic stress responses and participate in cross-talk with ROS production activities (Kobayashi et al. 2007). Transcription factors belonging to different families, such as WRKY, bZip, MYB, DREB, NAC, and AP2, are induced by Cd in different plant species (Herbette et al. 2006; Weber et al. 2006; Ogawa et al. 2009) . The inductions by Cd of transcripts for bZIP, MYB, and zinc finger transcriptional factors have also been demonstrated in the root of the metal accumulator B. juncea (Fusco et al. 2005). Genes involved in hormone signaling, mainly ABA and ethylene and jasmonic acid, have also been shown to be regulated in response to Cd (Herbette et al. 2006; Minglin et al. 2005) .

5.3 Cellular Detoxification and Repair

Several genes associated with cellular detoxification and repair have been shown to be induced by treatment with cadmium. Chitinases and heat shock proteins (HSPs) are induced in response to heavy-metal stress and are regarded as a second line of defense under these stress conditions (Metwally et al. 2003; Békésiová et al. 2008; Rodríguez-Serrano et al. 2009; Zhao et al. 2009). Transgenic plants expressing fungal chitinases actually showed enhanced tolerance to metals (Dana et al. 2006) , while chitinase isoforms are differentially modified by certain metals (Békésiová et al. 2008) . Chitinases are regulated by ROS and are possibly part of the general defense response program of cells under heavy-metal stress (Békésiová et al. 2008; Rodríguez-Serrano et al. 2009) . Other pathogenesis-related proteins (PRPs) are upregulated by Cd (Fusco et al. 2005; Rodríguez-Serrano et al. 2009). ROS-dependent up-regulation of PRP4A has been demonstrated in pea plants exposed to Cd, whose transcripts were specifically accumulated in palisade mesophyll cells, as evidenced by in situ hybridization (Rodríguez-Serrano et al. 2009). These results point to an overlap in the regulatory mechanisms underlying these processes, with ROS production being a common event in these situations.

HSPs are upregulated by heat stress and can act as molecular chaperones favoring the transport of proteins to organelles and preventing protein aggregation (Ma et al. 2006) . Induction of HSPs by Cd has been observed in different plant species (Sanitá di Toppi and Gabbrielli 1999; Rodríguez-Serrano et al. 2009) and is regulated by H2O2 overproduction (Rodríguez-Serrano et al. 2009). The transcription factors involved in HSP expression can act as H2O2 sensors (Miller and Mittler 2006) . In B. juncea, Cd upregulates a DNAJ HSP (BjCdR57), a chaperone involved in protein protection against stress, which confirms that protein denaturation is one of the effects of Cd toxicity (Suzuki et al. 2001; Fusco et al. 2005). GSH S-transferases catalyze the conjugation of xenobiotics with GSH and participate in the removal of ROS and are upregulated in response to Cd (Suzuki et al. 2002; Fusco et al. 2005; Ogawa et al. 2009). Antioxidative defenses such as glutaredoxin, thioredoxin, GSH reductase, monodehydroascorbate reductase, SOD, CAT, and POXs are upregulated by Cd in order to deal with oxidative damage caused by this metal (Lemaire et al. 1999; Herbette et al. 2006; Romero-Puertas et al. 2007a, b; Smeets et al. 2005; Ogawa et al. 2009) . Enzymes involved in vitamin E biosynthesis are upregulated in response to Cu and Cd in Arabidopsis plants, while vitamin E-deficient mutants (vtel) showed enhanced oxidative stress and sensitivity to both metals, suggesting that Vitamin E also contributes to defense against heavy metals (Collin et al.

2008). The regulation of these antioxidative enzymes is mainly dependent on H2O2 (Romero-Puertas et al. 2007a, b; Rodríguez-Serrano et al.

2009), although GSH metabolism also plays an important role in controlling the gene regulation of antioxidants in response to Cd stress (Cuypers et al. 2011). The activity of glucose-6-P dehydro-genase (G6PDH), malic enzyme (ME), and

NADP isocitrate dehydrogenase (NADP-ICDH) is stimulated by Ni, Zn, and Cd (Van Assche and Clijsters 1990; León et al. 2002), while, in pepper cultivars with different levels of sensitivity to Cd, tolerance to this heavy metal was more dependent on the availability of NADPH than on its antioxidant capacity (León et al. 2002) .

5.4 Metal Transporters

Some of the genes regulated by Cd, such as AtPcr1 (Song et al. 2004) and those belonging to the ABC, MATE, cation diffusion facilitator (CDF), heavy metal P-type ATPase (HMA) and ZIP families, are involved in Cd transport (Ogawa et al. 2009). Fe and Zn transporters are also often involved in Cd transport because of their low substrate specificity. The iron transporters ZIP, AtIRT1, OsIRT1111, and OsIRT2 as well as the Zn transporter OsZIP1 have been shown to transport Cd. The HMA family is also involved in Cd detoxification in addition to CDF transporters and natural resistance-associated macrophage protein (NRAMP) family transporters (Ogawa et al. 2009) . Pleiotropic drug resistance (PDR) family proteins are involved in Cd tolerance via export out of the cytoplasm (Kim et al. 2007). AtPDR8 is a cadmium extrusion pump, while AtOSA1 could be involved in the signal trans-duction pathway in response to oxidative stress (Kim et al. 2007; Jasinski et al. 2008). Cd-binding proteins such as Cdl19 could be involved in maintaining heavy-metal homeostasis and/or detoxification (Suzuki et al. 2002) .

5.5 Cell Wall Metabolism

The cell wall is one of the first structures to be directly exposed to Cd and has the ability to bind metals, which is regarded as a mechanism of metal tolerance. Most of the heavy metals associated with the cell wall are linked to polygalactur-onic acids, whose metal ion affinities vary depending on the metal in question. The plant cell wall is mainly composed of cellulose and matrix polysaccharides, which are divided into pectins and hemicelluloses, both of which are rich in polygalacturonic acids (Xiong et al. 2010). Cellulose is a key component in plant cell walls, and it has been reported that NO affects the cellulose content of tomato roots in a dose-dependent manner. Low concentrations of sodium nitroprus-side (SNP) increase cellulose content in roots, while higher concentrations have the opposite effect (Correa-Aragunde et al. 2008). Exogenous NO increases Cd tolerance in rice plants by increasing pectin and hemicelluloses content in the root cell wall and by decreasing Cd accumulation in the soluble fraction of cells in rice leaves ( Xiong et al. 2009) . H2O2 may also trigger secondary defenses, causing cell wall rigidification and lignifications in Cd-exposed cells (Schützendübel and Polle 2002). The transcript levels of genes involved in cell wall metabolism are modulated in response to Cd. The proteins involved in lignification and extension were therefore upregulated (Fusco et al. 2005; Herbette et al. 2006), whereas expansins and pectin esterases were downregulated (Herbette et al. 2006) .

5.6 Sulfate and GSH Metabolism

One of the best described mechanisms induced under heavy-metal toxicity is the chelation of the metal by PCs and GSH. PCs have the general formula (yGlu-Cys)n-Gly (with n = 2-11) and are synthesized enzymatically through the transpep-tidation of gGlu-Cys moieties of GSH onto another GSH molecule by the phytochelatin syn-thase (PCS) enzyme, which is known to be activated posttranslationally by a range of heavy metal metalloids (Grill et al. 2006) . Chelation of metals by PCs and the compartmentalization of PC-metal complexes in vacuoles (Clemens 2006; Grill et al. 2006) are generally considered as firstline defense mechanisms.

The rate-limiting step for PCs and GSH biosynthesis is the availability of reduced sulfur to the roots. Various genes involved in the sulfate metabolism are induced in response to Cd, which include sulfate transporters from roots (Sultr1; 1; Sultr1; 2), enzymes involved in sulfate reduction to sulfide (ATP sulfurylase), and those involved in PC biosynthesis (PC synthases) (Herbette et al. 2006; Ramos et al. 2007). One of the steps in PC biosynthesis is the synthesis of cysteine catalyzed by 0-acetylserine(thiol)lyase (OASTL) which is upregulated by Cd (Fusco et al. 2005). Arabidopsis plants over expressing OASTL were highly Cd resistant, which suggests that cysteine pool required for GSH biosynthesis is one of the principal factors affecting Cd tolerance (Dominguez-Solis et al. 2001). A deficiency in the major OASTL isoform in the cytosol from Arabidopsis plants, OAS-A1, causes aH2O2 homeostasis imbalance (Lopez-Martin et al. 2008).

5.7 Hydric Balance

The plant-water balance is also disturbed by Cd, and the stomatal opening is inhibited (Poschenrieder et al. 1989; Sandalio et al. 2001; Perfus-Barbeoch et al. 2002). Sequence analysis of Cd-responsive genes in the metal accumulator B. juncea revealed the induction of genes encoding aquaporins, which facilitates the movement of water through cellular membranes. In addition, other drought and ABA-responsive genes, such as BjCdR39 (the aldehyde dehydrogenase) and BjCdR55, (RNA-binding protein), are also upreg-ulated by Cd, which confirms the existence of cross-talk between Cd-induced and water stress-induced signaling using ABA as a signal transducer. Stomatal closure, a symptom of water stress mediated by ABA, is one of the principal responses of higher plants to Cd (Sanita di Toppi and Gabbrielli 1999).

5.8 Protein Degradation

Oxidative damage to proteins has been observed in different plant species exposed to Cd and is regarded as an oxidative stress marker (Sandalio et al. 2001; Pena et al. 2007; Djebali et al. 2008; Paradiso et al. 2008). Some of the proteins undergoing oxidative modification have been identified in pea leaves and include CAT, GR, Rubisco, and Mn-SOD (Romero-Puertas et al. 2004). Increased proteolytic activity in leaves following Cd treatment and more efficient degradation of the oxidized proteins have been observed (McCarthy et al. 2001; Romero-Puertas et al. 2004). Similar results have been reported by Pena et al. (2006) in Helianthus annus and by Djebali et al. (2008) in Solanum lycopersicum. A proteomic study of A. thaliana cells has also reported an increase in several proteases after Cd treatment (Sarry et al. 2006). Cd treatment has also been shown to increase polyubiquitinated protein accumulation (Pena et al. 2007). The proteasome-ubiquitin system is the major proteolytic pathway in eukaryotes and is also involved in the depredation of oxidized proteins (Pena et al. 2007). The plant proteasome was upregulated at transcrip-tional and translational levels under oxidative conditions caused by cadmium stress (Pena et al. 2006, 2007; Djebali et al. 2008; Polge et al. 2009) . Using in vivo experiments with A. thaliana mutants, it has been demonstrated that 20S proteasomes are preferentially involved in the degradation of oxidized proteins (Kurepa et al. 2008) . The remobilization of oxidized proteins may be a protective mechanism under stress conditions to prevent further damage to other macromolecules and to facilitate the recycling of amino acids for protein biosynthesis.

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